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In vitro Cell Migration and Invasion Assays
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MKK3 modulates JNK-dependent cell migration and invasion

Yihao Sun1, Di Zhang1, Xiaowei Guo1

  • 1The First Rehabilitation Hospital of Shanghai, Shanghai Key Laboratory of Signaling and Diseases Research, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China.

Cell Death & Disease
|February 17, 2019
PubMed

Insights

The study identifies MKK3 licorne (lic) as a key regulator of JNK-dependent cell migration and invasion. This finding, demonstrated in Drosophila, reveals a conserved mechanism in human cells and has implications for understanding cancer progression.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • The c-Jun N-terminal kinase (JNK) pathway is crucial for cell migration and invasion.
  • Identifying regulators of JNK-mediated cell migration is vital for understanding physiological and pathological processes.

Purpose of the Study:

  • To identify novel regulators of JNK-dependent cell migration using a genetic screen in Drosophila.
  • To investigate the role of MKK3 licorne (lic) in JNK-mediated cell migration and invasion.

Main Methods:

  • Genetic screen in Drosophila wing epithelia to identify factors regulating cell polarity-triggered cell migration.
  • Analysis of MKK3 licorne's function in Drosophila eye discs and thorax development.
  • Investigating the molecular mechanism of MKK3 licorne in JNK signaling activation and downstream target regulation.

Main Results:

  • MKK3 licorne (lic) was identified as an essential regulator of JNK-mediated cell migration and invasion.
  • Loss of lic suppressed JNK-triggered cell migration and Ras-induced tumor invasion.
  • Ectopic expression of lic induced JNK-mediated cell migration independently of p38 MAPK and promoted tumor invasion.
  • Lic activates JNK signaling, up-regulating MMP1 and integrin, hallmarks of epithelial-mesenchymal transition (EMT).
  • Human MKK3 expression in Drosophila recapitulated these effects and rescued defects.

Conclusions:

  • MKK3 licorne is a novel and evolutionarily conserved regulator of JNK-dependent cell migration and invasion.
  • This study provides in vivo evidence for MKK3's role in JNK signaling, challenging previous assumptions about its specificity for p38 MAPK.
  • The findings have implications for understanding cancer metastasis and developmental processes involving cell migration.

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